The field of social neuroscience is filling the gap between behavioral neuroscience and social psychology, employing experimental animal and human studies together with molecular and cellular approaches. For several decades, investigators have been exploring mechanisms of social affiliation that rely upon the neuropeptide oxytocin (OT). Together with vasopressin (VP), both peptide molecules are synthesized and released from the hypothalamus and selectively expressed in the brain, under the influence of gonadal steroids, seasonality and gender. The net effects in particular of OT, in regards to parenting, mating, and other social affiliation behaviors in mammals, have been assembled from species-specific components, defining the social life of the particular species under consideration. The speculative role of OT in human maternal-infant bonding behavior has recently been explored.
The OT system has experienced a remarkable resurgence departing from its role in the simple regulation of uterine contractions during labor and mild ejection during nursing. First recognized as an important mediator of learning and memory, and later in the formation of pair bonds between animal prairie vole mates, the primacy of OT in nurturing was first suggested in postpartum rats in which maternal behavior was initiated only after parturition. Maternal behavior was also experimentally evoked in adult virgin females primed with estrogen and injected centrally with OT, whereupon they proceeded to build nests and crouch over pups in a nursing posture. Experimental OT receptor antagonists were able to block the natural postpartum onset of maternal behavior in the rats. And as exogenous estrogen increased OT receptor expression in selective nuclei of the brain, there was both a local increase in OT receptors and pulsatile central release of the OT peptide during parturition.
Yet doubts of the primacy of OT in the initiation of maternal behavior surfaced when experimentally-induced OT null mutants, known as OT deficient (Oxt -/-) knock out (OT-KO) mice, displayed impairments in mild ejection and social recognition, with intact parturition and largely preserved maternal behaviors. Further, genetically engineered female mice lacking the OT brain receptor (Oxtr -/-) showed deficits in maternal behavior with longer latencies in retrieving their pups or crouching over them. Virgin Oxtr -/- females displayed a similar phenotype suggesting that the OT receptor is required for maternal nurturing outside the physiological context of pregnancy and parturition, and that other endogenous ligands, such as VP, could be activating this receptor in mice. Mice, unlike rats, that are promiscuously maternal since they do not require parturition or steroid induction to exhibit maternal care, illustrate obvious differences in the OT neural circuit. By comparison, OT may be critical in female rats to overcome their avoidance of neonates, thus allowing maternal behavior to emerge. Nonetheless, across species, and between mice and rats, there may be profound difference in the forebrain distribution of OT receptors even in the absence of any difference in the distribution or quantity of OT cells, making receptor maps a useful guide for social neuroscience behaviorists.
However its role in promoting parental attachment has been inferentially advanced by tagging single nucleotide polymorphisms (SNPs) to OXT/Neurophysin-I, OXTR and CD38. CD38 is a transmembrane receptor with high expression in the brain and an obligatory role in central OT release due to its association with adenosine diphosphate-ribosyl cyclase activity that mobilizes downstream intracellular calcium signaling. Thus, mothers carrying the OXTR SNP rs53576GG genotype engaged in more sensitive interactions with their infants, while two Neurophysin-I (OXT) SNPs, rs2740210 and rs4813627, were associated with mothers vocalizations during mother-infant interactions. A study of 323 mothers, fathers, and nonparents showed that risk alleles on OXTR (rs2254298, rs1042778) and CD38 (rs3796863) genes were associated with less parental touch. Moreover, the interaction of high plasma OT and low-risk CD38 alleles predicted longer durations of parent-infant gaze synchrony. Parents who reported more optimal caregiving in childhood had greater plasma OT, low-risk CD38 alleles, and more touch toward their infants. Following parents and their first born infants from birth to 3 years, parents’ behavioral synchrony at 1 and 6 months and mothers’ CD38 allele predicted children’s social reciprocity during interactions with their best friend at 3 years, indicating that the transfer from parent-infant attachment to attachment with close friends was supported by OT-pathway genes mediated by parenting behavior. Concluding that the OT-signaling in the brain is a unique determinant of parenting behavior or the modulator thereof, would be incorrect, since similar extrapolations have been proposed for a variety of social cognitive and emotional competencies including romantic couple relationships, friendship, and empathy.
Recognizing that research utilizes adults’ retrospective accounts of early caregiving with accounts that may be colored by the current emotional or physical state, more objective research is needed including critical observations employing prospective longitudinal designs and integrating information from imaging, genetic, and neuroendocrine biomarkers, combined with careful assessments to understand the involvement of OT-pathway genes in early parenting environments.